Association of serum brain-derived neurotrophic factor with hepatic enzymes, AST/ALT ratio, and FIB-4 index in middle-aged and older women

PLoS One. 2022 Aug 23;17(8):e0273056. doi: 10.1371/journal.pone.0273056. eCollection 2022.

Abstract

Substantial evidence suggests an important role of liver function in brain health. Liver function is clinically assessed by measuring the activity of hepatic enzymes in the peripheral blood. Brain-derived neurotrophic factor (BDNF) is an important regulator of brain function. Therefore, we hypothesized that blood BDNF levels are associated with liver function and fibrosis. To test this hypothesis, in this cross-sectional study, we investigated whether serum BDNF concentration is associated with liver enzyme activity, aspartate aminotransferase (AST)/ alanine aminotransferase (ALT) ratio, and fibrosis-4 (FIB-4) index in middle-aged and older women. We found that serum BDNF level showed a significant positive association with ALT and γ-glutamyltranspeptidase (GGT) activity and negative association with FIB-4 index, and a trend of negative association with the AST/ALT ratio after adjustment for age. Additionally, these associations remained statistically significant even after adjustment for body mass index (BMI) and fasting blood glucose level. These results demonstrate associations of serum BDNF levels with liver enzymes and hepatic fibrosis-related indices, which may underlie liver-brain interactions.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Alanine Transaminase
  • Aspartate Aminotransferases
  • Brain-Derived Neurotrophic Factor / blood*
  • Cross-Sectional Studies
  • Female
  • Humans
  • Liver Cirrhosis / diagnosis
  • Liver*
  • Middle Aged

Substances

  • Brain-Derived Neurotrophic Factor
  • BDNF protein, human
  • Aspartate Aminotransferases
  • Alanine Transaminase

Grants and funding

This research was funded by the Japan Society for the Promotion of Science Grants in Aid for Scientific Research (No. 16J10577, 19K24330, and 20K19498 to Takumi Yokokawa and 17H02183 to Satoshi Fujita). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.